VSIG10L (V-set and immunoglobulin domain containing 10 like) encodes a membrane-bound protein with immunoglobulin (Ig)-like domains. In the esophageal mucosa, VSIG10L is selectively expressed in the suprabasal squamous cells and is essential for epithelial maturation and homeostasis. Loss of esophageal VSIG10L expression is observed frequently in patients with chronic gastroesophageal reflux disease (GERD), a known risk factor for Barrett&rsquo;s esophagus (BE). Patients with BE, in particular, are at a high risk of developing esophageal adenocarcinoma (EAC). Vsig10l KO mice carry a CRISPR/cas9-generated knock-out mutation in which all 10 exons of the mouse Vsig10l gene have been deleted. This knock-out model's deleterious frameshift mutations are found in familial BE/EAC patients. Mice carrying human-orthologous germline mutations in Vsig10l exhibit loss of desmosomes, concomitant with disrupted epithelial differentiation programs, in the squamous mucosa. Upon long-term exposure to a bile acid (deoxycholate) supplemented diet, Vsig10l-mutant mice develop overt BE-like lesions in the forestomach.

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Vsig10l KO mice harbor a targeted deletion of exons 1-10 of the mouse Vsig10l (V-set and immunoglobulin domain containing 10 like) gene, resulting in a loss of Vsig10l expression. This strain is useful in studies of squamous mucosa/cell biology and associated diseases, including cancer.